Beyond the microsatellite instability phenotype as a cause of a high tumor mutational burden (TMB) and a marker of response to immune checkpoint inhibition [5, 6], diagnostic mutation profiling is currently limited to KRAS/NRAS (RAS) exons 2–4, which are mutations associated with resistance to monoclonal anti-EGFR antibodies, and to BRAFV600E as a target for combination therapies [7]. The gene discussed is KRAS; the disease is neoplasm.